| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5952020 | Cardiovascular Pathology | 2012 | 8 Pages |
Abstract
Our data suggest that, in the ARVC heart, plakoglobin is mainly redistributed from the junctions to other cellular pools and that protein degradation only plays a secondary role. Homogenous changes in the phosphorylation status of connexin43 were observed in multiple ARVC samples, suggesting that this might be a general feature of the disease.
Keywords
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Authors
Katja Gehmlich, Petros Syrris, Mareike Reimann, Angeliki Asimaki, Elisabeth Ehler, Alison Evans, Giovanni Quarta, Antonis Pantazis, Jeffrey E. Saffitz, William J. McKenna,